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Human Polyclonal ube3a Primary Antibody pour IP, WB - ABIN153040
Jiang, Sahoo, Michaelis, Bercovich, Bressler, Kashork, Liu, Shaffer, Schroer, Stockton, Spielman, Stevenson, Beaudet: A mixed epigenetic/genetic model for oligogenic inheritance of autism with a limited role for UBE3A. dans American journal of medical genetics. Part A 2004
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Human Polyclonal ube3a Primary Antibody pour IHC (p), ELISA - ABIN545148
Be, Hong, Wei, Androphy, Chen, Baleja: Solution structure determination and mutational analysis of the papillomavirus E6 interacting peptide of E6AP. dans Biochemistry 2001
Show all 3 Pubmed References
Human Monoclonal ube3a Primary Antibody pour IF, IHC (p) - ABIN563326
Underbrink, Howie, Bedard, Koop, Galloway: E6 proteins from multiple human betapapillomavirus types degrade Bak and protect keratinocytes from apoptosis after UVB irradiation. dans Journal of virology 2008
Human Polyclonal ube3a Primary Antibody pour WB - ABIN153039
Sato, Stryker: Genomic imprinting of experience-dependent cortical plasticity by the ubiquitin ligase gene Ube3a. dans Proceedings of the National Academy of Sciences of the United States of America 2010
Human Monoclonal ube3a Primary Antibody pour IF, IHC (p) - ABIN2477024
Wolyniec, Shortt, de Stanchina, Levav-Cohen, Alsheich-Bartok, Louria-Hayon, Corneille, Kumar, Woods, Opat, Johnstone, Scott, Segal, Pandolfi, Fox, Strasser, Jiang, Lowe, Haupt, Haupt: E6AP ubiquitin ligase regulates PML-induced senescence in Myc-driven lymphomagenesis. dans Blood 2012
Analysis of ubiquitin recognition by the HECT ligase E6AP provides insight into its linkage specificity.
Excessive UBE3A dosage was found to impair retinoic acid-mediated neuronal homeostatic synaptic plasticity. The autism spectrum disorders-like symptoms were recapitulated in mice by overexpressing UBE3A in the prefrontal cortex.
Mechanistic dissection further disclosed that RYBP directly binds to ubiquitin protein ligase E3A (UBE3A) to promote its ubiquitination and proteasomal degradation in an autoubiquitination-independent manner
Two Angelman syndrome point mutations of UBE3A that affect the AZUL domain show an impaired ability to bind PSMD4.
molecular docking demonstrated that quercetin binds stably in the central pocket of E6, the binding site of E6AP. These data suggest that quercetin increases the nuclear localization of p53 by interrupting E6/E6AP complex formation in cervical cancer cells.
UBE3A start codon variant is associated with Angelman syndrome.
Overall, results from this study provide insight into the potential biological pathways controlled by E6AP in prostate cancer cells and identifies clusterin as a novel target of E6AP.
Using human neuroblastoma SH-SY5Y cells in culture, we also observed that human DDI1 is ubiquitinated by UBE3A, without being targeted for degradation.
High UBE3A expression is associated with Liver Tumorigenesis.
These data provide structural and functional insights into the dynamics of the full-length E6AP-E6-p53 enzyme-substrate complex.
UBE3A regulates an imprinted gene network involving DNA methylation and H2A.Z deposition.
ANCR overexpression inhibited NSCLC cell migration and invasion and downregulated TGF-beta1 expression, while TGF-beta1 treatment showed no significant effects on ANCR expression but promoted NSCLC cell migration and invasion.
Results from a study on gene expression variability markers in early-stage human embryos shows that UBE3A is a putative expression variability marker for the 3-day, 8-cell embryo stage.
The divergence of E6 proteins from either MAML1 or E6AP binding preference is a major event in papillomavirus evolution.
Data report the establishment and thorough characterization of a new iPSC line from a patient with Angelman syndrome, harboring a defined three-base pair deletion within the maternally inherited UBE3A allele. Using computer modeling of the mutant protein, a local destabilization around the catalytic cleft of UBE3A was proposed, likely impairing the binding of substrates.
We demonstrate that E6AP regulates p27 expression by inhibiting its transcription in an E2F1-dependent manner. Concomitant knockdown of E6AP and p27 partially restores PC cell growth, supporting the contribution of p27 to the overall effect of E6AP on prostate tumorigenesis.
novel IVS15-1G>C and c.2540 C>T mutations of the UBE3A gene probably underlie the AS in the two families
Findings show neuronal overexpression of Ube3a isoform 2 causes phenotypes translatable to neurodevelopmental disorders.
This study demonstrate the importance of the N-terminal domain of full length E6AP for diubiquitin chain specificity.
our data demonstrates that E6AP facilitates ubiquitination and subsequent degradation of G-CSFR leading to attenuation of its downstream signaling and inhibition of granulocytic differentiation.
our findings elucidate the mechanisms underlying the subcellular localization of UBE3A, and indicate that the nuclear UBE3A isoform is the most critical for the pathophysiology of Angelman syndrome
Ube3a reinstatement mitigates epileptogenesis in Angelman syndrome model mice.
In a mouse model of Angelman Syndrome, restoring UBE3A levels in adult animals fully rescued all the identified physiological deficits of mPFC neurons. Moreover, the kinetics of reversing these synaptic deficits closely followed the reinstatement of UBE3A protein level.
Data suggest that differences seen in electroencephalographic (EEG) abnormalities may be due to differences between models and exons targeted for disruption in ubiquitin protein ligase E3A (Ube3a).
Here the authors report that Ube3a regulates mTORC1 signaling by targeting p18, a subunit of the Ragulator. Ube3a ubiquitinates p18, resulting in its proteasomal degradation.
E6AP is partially redistributed from the nucleus to the cytoplasm in encephalomyocarditis virus-infected cells, thereby increasing its availability to participate in cytoplasmic encephalomyocarditis virus replication processes.
We found that in primary neurons and in Ube3A transgenic autism mouse brain, overexpression of E6AP leads to significant loss of dendritic arborization
These data present a proof of principle that the transcriptional coactivation function of E6AP may have a crucial role in the pathobiology of Angelman syndrome.
Paternal UBE3A also partially colocalizes with a marker of neural progenitors, SOX2, implying that relaxed or incomplete imprinting of paternal Ube3a reflects an overall immature molecular phenotype
Using in vivo patch-clamp electrophysiology, study measured the visually evoked responses to square-wave drifting gratings in L2/3 regular-spiking (RS) neurons in control mice, Ube3a-deficient mice (Angelman syndrome model), and mice in which Ube3a was conditionally reinstated in GABAergic neurons; found that Ube3a-deficient mice exhibited enhanced pyramidal neuron excitability in vivo as well as weaker orientation tuning
Findings suggest that aberrant function of Ube3a could influence the progression of AD and restoring normal level of Ube3a might be beneficial for AD.
Encephalomyocarditis virus (EMCV) 3C protease accumulates to higher levels in EMCV-infected E6AP knockdown cells than in control cells, indicating a role for E6AP in in vivo 3C protease concentration regulation.
The expression of three tumor suppressor genes encoded in the INK4/ARF locus (p15(INK4b), p16(INK4a), and p19(ARF)) was decreased in E6AP(-/-) embryo fibroblasts.
Maternal loss of Ube3a affects nociception via a central, but not peripheral mechanism.
Our findings suggest that UBE3A may act locally to regulate individual synapses while also mediating global, neuronwide influences through the regulation of gene transcription
treatment of topotecan, a brain-penetrating topoisomerase 1 inhibitor, to HD transgenic mouse considerably improved its motor behavioural abnormalities. Finally, we show that topotecan treatment to HD mouse not only inhibits the expression of transgenic mutant huntingtin, but also at the same time induces the expression of Ube3a
We report that mice with maternally-inherited deletions of Ube3a that models Angelman syndrome show an increased social preference/interaction.
increasing UBE3A in the nucleus downregulates the glutamatergic synapse organizer Cbln1, which is needed for sociability in mice
Drosophila endogenously expresses Dube3a (fly UBE3A homolog) in glial cells and neurons. A robust seizure-like phenotype was observed in flies overexpressing Dube3a in glial cells, but not neurons. Glial-specific knockdown of ATPalpha also produced seizure-like behavior, and this phenotype was rescued by simultaneously overexpressing ATPalpha and Dube3a in glia.
Negative regulation of Tkv by Ube3a was conserved in mammalian cells. These results reveal a critical role for Ube3a in regulating NMJ synapse development by repressing BMP signaling. This study sheds new light onto the neuronal functions of UBE3A and provides novel perspectives for understanding the pathogenesis of UBE3A-associated disorders.
Data indicate that E3 ligase called ube3 (dube3a) is required for brain development as mutants have defective mushroom bodies.
Rpn10 is targeted for degradation by Ube3a.
In Drosophila melanogaster the human homologue ube3a regulates the actin cytoskeleton and neuronal homeostasis.
MeCP2 and E6AP play a role in the transcriptional control of common target gene expression.
Ube3a regulates serotonin and dopamine synthesis in the fly brain by increasing GTP cyclohydrolase I activity.
dube3a null mutants appear normal externally, but display abnormal locomotive behavior and circadian rhythms, and defective long-term memory; overexpression in the nervous system caused locomotion defects, dependent on the ubiquitin ligase activity
Overexpression of dUBE3A decreased dendritic branching.
In the skeletal muscle of neonate pigs, both NECD and SNRPN were maternally imprinted, while UBE3A was not imprinted.
This gene encodes an E3 ubiquitin-protein ligase, part of the ubiquitin protein degradation system. This imprinted gene is maternally expressed in brain and biallelically expressed in other tissues. Maternally inherited deletion of this gene causes Angelman Syndrome, characterized by severe motor and intellectual retardation, ataxia, hypotonia, epilepsy, absence of speech, and characteristic facies. The protein also interacts with the E6 protein of human papillomavirus types 16 and 18, resulting in ubiquitination and proteolysis of tumor protein p53. Alternative splicing of this gene results in three transcript variants encoding three isoforms with different N-termini. Additional transcript variants have been described, but their full length nature has not been determined.
CTCL tumor antigen se37-2
, E6AP ubiquitin-protein ligase
, human papilloma virus E6-associated protein
, human papillomavirus E6-associated protein
, oncogenic protein-associated protein E6-AP
, renal carcinoma antigen NY-REN-54
, ubiquitin-protein ligase E3A
, ubiquitin protein ligase E3A (human papilloma virus E6-associated protein, Angelman syndrome)
, ubiquitin protein ligase E3A
, E6-AP ubiquitin protein ligase
, ubiquitin conjugating enzyme E3A
, drosophila angelman syndrome
, angelman syndrome
, ubiquitin-protein ligase E3A-like